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Pharm U6 Terms
Pharmacology: Unit 6 Terms
| Question | Answer |
|---|---|
| Endocrine system | body system that regulates other body systems; glands release hormones into the bloodstream |
| Hormones | released into bloodstream; have slow onset and long duration of action |
| Negative feedback system | all hormone secretion is regulated by this mechanism |
| Hyperfunction of the endocrine system | where too much of a hormone is secreted or produced, or side effects are occurring from medication for hypofunction; thyrotoxicosis, hyperglycemia, hyperthyroidism, hyperparathyroidism, Cushing’s disease |
| Hypofunction of endocrine system | where not enough hormone is secreted/produced or side effects occurring from hyperfunction medications; Addison’s disease, cretinism, hypoparathyroidism, hypoglycemia, hypothyroidism |
| Diabetes mellitus | genetically influenced metabolic disorder of carbohydrate, fat, and protein metabolism characterized by high BGL due to inadequate/absent insulin production and/or impaired insulin action |
| Type 1 Diabetes Mellitus | immune mediated (formerly insulin dependent); genetic susceptibility with environmental exposure (virus, infection) leading to abnormal autoimmune response and destruction of insulin producing pancreatic beta cells |
| Type 1 Diabetes Mellitus | family history of autoimmune disorders, Islet cell antibodies, insulin autoantibodies, absence of C-peptide; occurs more often in those <20yo, European ancestry; 10-15% of diabetics are this type |
| Type 2 Diabetes Mellitus | adult or maturity onset; may range from predominantly insulin resistant w/ relative insulin deficiency to predominantly insulin secretory defect with insulin resistance |
| Type 2 diabetes mellitus | strong genetic autosomal dominant familial pattern; impaired insulin production response of beta cells to demands of obesity; insulin resistance mediated by decreased insulin receptors; post cell receptor defect impairing glucose transport |
| Type 2 diabetes mellitus risk factors | family history of diabetes, identification as glucose intolerant, African-American, Asian American, Hispanic American, Native American, Pacific Islander; Age >45, obesity, giving birth to infant >9lbs |
| Syndrome X—Metabolic syndrome (Diabesity) | cluster of disorders which may include hypertension (BP >130/85), fasting BGL >110; abnormal lipid profile, truncal obesity, insulin resistance, hyperinsulinism |
| Impaired fasting glucose (IFG) | glucose levels fall between normal and overt diabetes; may worsen over time, remain unchanged, or revert to normal |
| Gestational diabetes mellitus | diabetes during pregnancy; women should be tested at 24 to 28 weeks with a 50g glucose load |
| Diabetes mellitus | about 8 million diagnosed cases and about 8 million undiagnosed cases; after thyroid disease and obesity most common metabolic disorder in primary care; third leading cause of death in the US. |
| Type I signs and symptoms | usually sudden and severe in onset; early Polyuria, Polydipsia, Polyphagia; weight loss w/ increased appetite, blurred vision, fatigue, nausea, rashes |
| Type 1 advanced disease and long-term complications | microvascular and neurogenic changes; paresthesias, progressive visual impairment, cold extremities; decreased pedal pulses, nocturia, neurogenic bladder, uremia, impotence |
| Type 2 signs and symptoms | onset more insidious, early may not be noticed; Polyuria, Polydipsia, Polyphagia; blurred vision, fatigue, slow healing sores, recurrent infections, spontaneous abortion |
| Type 2 advanced disease/long-term complications | macrovascular changes prominent; atherosclerosis, vascular inefficiency, coronary heart disease; hyperosmolar, hyperglycemic, nonketotic coma |
| Type 1 physical findings | thin, ill looking, orthostatic hypotension, skin infections/ulcerations; retinopathy with exudates, cardiovascular problems, neurologic sensory loss, absent knee and ankle jerks, deficits in extraocular movements |
| Type 2 physical findings | usually obese, hypertension; advanced disease includes skin ulcerations, retinopathy, cardiovascular problems, sensory loss |
| Diagnosis of diabetes mellitus | plasma blood sugar criteria; if FBS>126 and is >126 on repeat testing OR if random non-fasting BGL is >200 and symptoms of 3 Ps with apparent weight loss |
| Urinalysis diagnosis | presence of glucose, acetone, and advanced stages of protein |
| Blood urea nitrogen and urine creatinine | elevated in acute dehydration and with renal involvement |
| Serum cholesterol and triglyceride levels | often elevated, especially in type 2 |
| Electrocardiogram and chest radiography | for coronary and pulmonary pathology |
| Hemoglobin A1C | predominantly used as measure of glycemic control; indicates average plasma glucose level for previous 60-90 days; tested every 3-6 months; 5.5 to 7% considered good control (normal range is 2.2 to 4.8) |
| Oral antidiabetic agents | used to treat type 2; control carbohydrate metabolism and decrease glucose levels |
| Oral hypoglycemic agents | stimulate the pancreas to secrete more insulin; not given in children or type 1 in whom beta cells do not function; administered to type 2. Newer agents sensitize body to insulin present |
| Sulfonylureas (secretagogues—induce secretions of another substance) | hypoglycemic agent; chemically related to sulfonamides but without antiinfective activity; enter + stimulate beta cells to synthesize and release insulin; bind to K channel of beta cells to allow influx of Ca ions |
| Oral hypoglycemic agents | 1st gen potent with long duration, increased risk of hypoglycemia, especially in elderly; precautions in those with renal, liver, or cardiovascular disease; risk of hypoglycemia and weight gain |
| Nonsulfonylureas (meglitinides) | hypoglycemic agent; secretagogues; stimulate insulin secretion from beta cells; more rapidly absorbed; onset of action 20-30 minutes with peak at 60 minutes, so must be taken 1 to 30 minutes before each meal |
| Biguanides | insulin resistance reducers; decrease liver glucose production & intestinal glucose absorption, lowers postprandial glucose levels; increases sensitivity of peripheral tissues to insulin; used as antihyperglycemic drug, keeps BGL from rising after eating |
| Biguanides | no direct effect on insulin secretion; causes moderate weight loss, improved lipid profile; low risk of hypoglycemia; side effects flatulence, diarrhea, contraindicated in renal, liver, advanced CV disease |
| Insulin sensitizers (thiazolidinediones—TDZs; glitazones) | directly target insulin resistance, enhance peripheral cell response to insulin, allows efficient glucose use; decreases insulin resistance/sensitivity to fats, skeletal muscle, liver cells; secondary effect suppression of hepatic glucose production |
| Insulin sensitizers (thiazolidinediones—TDZs; glitazones) | used for type 2 when glucose control inadequate with >30 units insulin/day in divided doses w/ food; increased risk of hypoglycemia; potential for drug interactions; new class of drugs not used by many patients; reversible elevation in liver enzymes |
| Glucose absorption inhibitors (alpha-glucosidase inhibitors) | interfere with brush border enzymes in small intestine that break down complex carbohydrates, so interfere with dietary carb digestion (hydrolase, alpha amylase); inhibit glycoside hydrolase so that glucose absorption delayed/eliminated |
| Glucose absorption inhibitors (alpha-glucosidase inhibitors) | used with oral hypoglycemia agents and insulin; lowers postprandial BGL; low risk of hypoglycemia or weight gain; less efficacious than sulfonylureas/biguanides |
| Combo product—glucovance | fixed combination of glyburide & metformin; decreases BGLs and A1C levels in greater amounts than glyburide or metformin monotherapy; primary advantage is patient compliance |
| Insulin | enhances transmembrane passage of glucose across cell membranes; used in confirmed or suspected type 1 or gestational diabetes; used in type 2 if other treatments don’t work; weight gain and need for frequent BGL monitoring can be troublesome |
| Rapid-acting insulin | insulin with short duration; about 15 minute onset |
| Short-acting insulin (Regular) | short duration with about 30 minute onset |
| Intermediate acting insulin (“N”) | longer duration of 8-12 hours; onset 30 minutes |
| Combination Insulin products – Isophane | combination of a percentage of intermediate acting and rapid acting insulin (humulin N and R 70/30) |
| Long acting insulin – glargine (Lantus) | basal acting insulin given daily at bedtime to adults and children with type 1 diabetes; onset of action is 1 to 2 hours; duration is 24 hours; cannot be mixed with any other insulin preparation |
| Causes of hypoglycemia | danger of insulin shock; insulin overdose, omission of meals, injection errors, heavy exercise, renal failure, weight loss, hepatitis, pituitary/adrenal insufficiency; drugs that affect insulin metabolism |
| Symptoms of hypoglycemia | weakness, sweating, shakiness, dizziness, headaches, hunger, irritability, convulsions, confusion, coma, tachycardia, palpitations |
| IV glucose | treatment of hypoglycemia |
| Causes of hyperglycemia | danger of diabetic coma; infection, trauma, myocardial infarction or other severe stress, noncompliance with treatment regimen |
| Symptoms of hyperglycemia | drowsiness, fruity breath, polyuria, rapid, deep breathing, nausea, vomiting, red, dry skin |
| IV insulin | treatment of hyperglycemia |
| Somogyi phenomenon | caused by morning rebound hyperglycemia; occurs in response to nocturnal hypoglycemia with excessive insulin administration |
| Somogyi clues | erratic plasma glucose and urine ketone values; symptoms of nocturnal hypoglycemia (night sweats, nightmares, low serum glucose) |
| Reduce insulin dose 10% to 20% | somogyi phenomenon treatment |
| Dawn phenomenon | early morning fasting hyperglycemia without nocturnal hypoglycemia; thought to be related to circadian rhythem secretion of growth hormone; treated by evening or bedtime dose of insulin |
| Lipodystrophy | atrophy/overgrowth at insulin injection sites; prevent by proper rotation of injection sites |
| Diabetic ketoacidosis (DKA) | hyperglycemia with ketonuria and disruption of the fluid, electrolyte, and pH balance leading to coma, death; marked by hyperglycemia, metabolic acidosis, ketonemia; sometimes presenting sign in undiagnosed type 1 |
| Diabetic ketoacidosis (DKA) causes | infection, trauma, myocardial infarction, other stress, noncompliance with therapeutic regimen |
| DKA treatment | emergency fluid replacement, insulin therapy, sodium bicarbonate therapy, close monitoring of blood chemistries |
| Hyperglycemic agents (glucose) | stimulate glucose synthesis to raise glucose level and provide immediate glucose for use; used for sever hyperglycemic states |
| Hyperglycemic agent side effects | hyperglycemia; polydipsia, polyuria, polyphagia; nausea, vomiting with low glucose level; coma |
Created by:
michellerogers
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